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Early oxidative stress in testis and epididymal sperm in streptozotocin-induced diabetic mice: its progression and genotoxic consequences.
Reprod Toxicol. 2007 Jun; 23(4):578-87.RT

Abstract

Experimental induction of diabetes mellitus in animal models using chemical diabetogens is demonstrated to impair testicular function progressively leading to decreased fertility. Although, both steroidogenic and spermatogenic dysfunctions have been reported, the role of oxidative stress mechanism/s has been less understood. We have investigated the induction of oxidative damage during early diabetic phase in testis and epididymal sperm (ES) in mice administered an acute dose of streptozotocin (STZ). Our results show enhanced lipid peroxidation in testis (cytosol and mitochondria) and ES and increased ROS production as early as 5 days. Further, significant perturbations in the activities of antioxidant enzymes in testis/ES and enhanced protein carbonyl content were suggestive of increased oxidative stress during early diabetic phase. STZ-induced oxidative damage in both compartments was amenable for attenuation by treatment with oral supplements of either ascorbic acid (10mg/(kg(bw)day)) or taurine (1g/(kg(bw)day)). Furthermore, the oxidative impairments in testis/ES were persistent during the progressive phase (as measured at 2 and 4 weeks of sampling) and were associated with significant increase DNA damage (testis) and higher incidence of abnormal sperms. Interestingly, mating of STZ treated males sequentially for a period of 5 weeks with virgin untreated females resulted in a significant increase in the male-mediated dominant lethal-type mutations during the first 3 weeks, indicating a stage-specific genotoxic effect on post-meiotic germ cells. Based on the occurrence of oxidative impairments in STZ-treated mice both during both early and progressive phase, it is hypothesized that oxidative stress mechanisms may be wholly or in part contribute towards the development of testicular dysfunction and degeneration under situations of experimentally induced diabetes in animal models.

Authors+Show Affiliations

Department of Biochemistry and Nutrition, Central Food Technological Research Institute, Mysore 570 020, India.No affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

17360155

Citation

Shrilatha, B, and Muralidhara. "Early Oxidative Stress in Testis and Epididymal Sperm in Streptozotocin-induced Diabetic Mice: Its Progression and Genotoxic Consequences." Reproductive Toxicology (Elmsford, N.Y.), vol. 23, no. 4, 2007, pp. 578-87.
Shrilatha B, Muralidhara . Early oxidative stress in testis and epididymal sperm in streptozotocin-induced diabetic mice: its progression and genotoxic consequences. Reprod Toxicol. 2007;23(4):578-87.
Shrilatha, B., & Muralidhara, . (2007). Early oxidative stress in testis and epididymal sperm in streptozotocin-induced diabetic mice: its progression and genotoxic consequences. Reproductive Toxicology (Elmsford, N.Y.), 23(4), 578-87.
Shrilatha B, Muralidhara . Early Oxidative Stress in Testis and Epididymal Sperm in Streptozotocin-induced Diabetic Mice: Its Progression and Genotoxic Consequences. Reprod Toxicol. 2007;23(4):578-87. PubMed PMID: 17360155.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Early oxidative stress in testis and epididymal sperm in streptozotocin-induced diabetic mice: its progression and genotoxic consequences. AU - Shrilatha,B, AU - Muralidhara,, Y1 - 2007/02/13/ PY - 2006/10/20/received PY - 2007/01/25/revised PY - 2007/02/05/accepted PY - 2007/3/16/pubmed PY - 2007/7/14/medline PY - 2007/3/16/entrez SP - 578 EP - 87 JF - Reproductive toxicology (Elmsford, N.Y.) JO - Reprod. Toxicol. VL - 23 IS - 4 N2 - Experimental induction of diabetes mellitus in animal models using chemical diabetogens is demonstrated to impair testicular function progressively leading to decreased fertility. Although, both steroidogenic and spermatogenic dysfunctions have been reported, the role of oxidative stress mechanism/s has been less understood. We have investigated the induction of oxidative damage during early diabetic phase in testis and epididymal sperm (ES) in mice administered an acute dose of streptozotocin (STZ). Our results show enhanced lipid peroxidation in testis (cytosol and mitochondria) and ES and increased ROS production as early as 5 days. Further, significant perturbations in the activities of antioxidant enzymes in testis/ES and enhanced protein carbonyl content were suggestive of increased oxidative stress during early diabetic phase. STZ-induced oxidative damage in both compartments was amenable for attenuation by treatment with oral supplements of either ascorbic acid (10mg/(kg(bw)day)) or taurine (1g/(kg(bw)day)). Furthermore, the oxidative impairments in testis/ES were persistent during the progressive phase (as measured at 2 and 4 weeks of sampling) and were associated with significant increase DNA damage (testis) and higher incidence of abnormal sperms. Interestingly, mating of STZ treated males sequentially for a period of 5 weeks with virgin untreated females resulted in a significant increase in the male-mediated dominant lethal-type mutations during the first 3 weeks, indicating a stage-specific genotoxic effect on post-meiotic germ cells. Based on the occurrence of oxidative impairments in STZ-treated mice both during both early and progressive phase, it is hypothesized that oxidative stress mechanisms may be wholly or in part contribute towards the development of testicular dysfunction and degeneration under situations of experimentally induced diabetes in animal models. SN - 0890-6238 UR - https://www.unboundmedicine.com/medline/citation/17360155/Early_oxidative_stress_in_testis_and_epididymal_sperm_in_streptozotocin_induced_diabetic_mice:_its_progression_and_genotoxic_consequences_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0890-6238(07)00030-5 DB - PRIME DP - Unbound Medicine ER -